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Gut Aug 2018Microbiota alterations are linked with colorectal cancer (CRC) and notably higher abundance of putative oral bacteria on colonic tumours. However, it is not known if...
BACKGROUND AND AIMS
Microbiota alterations are linked with colorectal cancer (CRC) and notably higher abundance of putative oral bacteria on colonic tumours. However, it is not known if colonic mucosa-associated taxa are indeed orally derived, if such cases are a distinct subset of patients or if the oral microbiome is generally suitable for screening for CRC.
METHODS
We profiled the microbiota in oral swabs, colonic mucosae and stool from individuals with CRC (99 subjects), colorectal polyps (32) or controls (103).
RESULTS
Several oral taxa were differentially abundant in CRC compared with controls, for example, and s pp. A classification model of oral swab microbiota distinguished individuals with CRC or polyps from controls (sensitivity: 53% (CRC)/67% (polyps); specificity: 96%). Combining the data from faecal microbiota and oral swab microbiota increased the sensitivity of this model to 76% (CRC)/88% (polyps). We detected similar bacterial networks in colonic microbiota and oral microbiota datasets comprising putative oral biofilm forming bacteria. While these taxa were more abundant in CRC, core networks between pathogenic, CRC-associated oral bacteria such as , and were also detected in healthy controls. High abundance of Lachnospiraceae was negatively associated with the colonisation of colonic tissue with oral-like bacterial networks suggesting a protective role for certain microbiota types against CRC, possibly by conferring colonisation resistance to CRC-associated oral taxa and possibly mediated through habitual diet.
CONCLUSION
The heterogeneity of CRC may relate to microbiota types that either predispose or provide resistance to the disease, and profiling the oral microbiome may offer an alternative screen for detecting CRC.
Topics: Adult; Aged; Case-Control Studies; Colonic Polyps; Colorectal Neoplasms; Feces; Female; Humans; Male; Microbiota; Middle Aged; Mouth; Sensitivity and Specificity
PubMed: 28988196
DOI: 10.1136/gutjnl-2017-314814 -
Cell Host & Microbe Jul 2017Host factors in the intestine help select for bacteria that promote health. Certain commensals can utilize mucins as an energy source, thus promoting their colonization....
Host factors in the intestine help select for bacteria that promote health. Certain commensals can utilize mucins as an energy source, thus promoting their colonization. However, health conditions such as inflammatory bowel disease (IBD) are associated with a reduced mucus layer, potentially leading to dysbiosis associated with this disease. We characterize the capability of commensal species to cleave and transport mucin-associated monosaccharides and identify several Clostridiales members that utilize intestinal mucins. One such mucin utilizer, Peptostreptococcus russellii, reduces susceptibility to epithelial injury in mice. Several Peptostreptococcus species contain a gene cluster enabling production of the tryptophan metabolite indoleacrylic acid (IA), which promotes intestinal epithelial barrier function and mitigates inflammatory responses. Furthermore, metagenomic analysis of human stool samples reveals that the genetic capability of microbes to utilize mucins and metabolize tryptophan is diminished in IBD patients. Our data suggest that stimulating IA production could promote anti-inflammatory responses and have therapeutic benefits.
Topics: Animals; Anti-Inflammatory Agents; Bacteria; Bacteroides; Clostridiales; Colon; Cytokines; Dysbiosis; Humans; Indoles; Inflammation; Inflammatory Bowel Diseases; Intestinal Mucosa; Intestines; Mice; Mucin-2; Mucins; Organoids; Peptostreptococcus; Symbiosis
PubMed: 28704649
DOI: 10.1016/j.chom.2017.06.007 -
Frontiers in Cellular and Infection... 2023The previous researches show that infertile patients have a higher incidence of endometritis and endometrial polyps, and the occurrence of these two diseases is related...
BACKGROUND
The previous researches show that infertile patients have a higher incidence of endometritis and endometrial polyps, and the occurrence of these two diseases is related to changes in the microbiota of the genital tract. We aim to determine the composition and changing characteristics of the microbiota in the genital tract (especially the endometrium) of infertile patients with chronic endometritis or endometrial polyps, and find the correlation between it and the occurrence of diseases.
METHODS
This is a prospective study. We collected genital tract biopsy samples from 134 asymptomatic infertile patients receiving assisted reproductive therapy before embryo transfer. Through pathological examination and 16S ribosomal RNA(16S rRNA) sequencing, we determined the distribution of chronic endometritis and endometrial polyps in these patients, as well as their distribution of reproductive tract microorganisms.
RESULTS
Compared with the normal control group, the microbial group of reproductive tract in patients with chronic endometritis and endometrial polyps is changed, and there are significant species differences and relative abundance differences in the vagina, cervix and uterine cavity. , the dominant flora of female genital tract, showed a change in abundance in patients with endometrial diseases. Endometrial microbiota composed of , etc. are related to chronic endometritis and endometrial polyps.
CONCLUSION
The results showed that, compared with the normal control group, the endometrial microbiota of infertile patients with chronic endometritis or endometrial polyps did have significant changes in the relative abundance distribution of species, suggesting that changes in local microecology may be an important factor in the occurrence of disease, or even adverse pregnancy outcomes. The further study of endometrial microecology may provide a new opportunity to further improve the diagnosis and treatment strategy of chronic endometritis.
Topics: Pregnancy; Humans; Female; Endometritis; RNA, Ribosomal, 16S; Prospective Studies; Infertility, Female; Endometrium; Microbiota
PubMed: 37284497
DOI: 10.3389/fcimb.2023.1125640 -
International Journal of Molecular... Nov 2020Several studies in recent times have linked gut microbiome (GM) diversity to the pathogenesis of cancer and its role in disease progression through immune response,...
Several studies in recent times have linked gut microbiome (GM) diversity to the pathogenesis of cancer and its role in disease progression through immune response, inflammation and metabolism modulation. This study focused on the use of network analysis and weighted gene co-expression network analysis (WGCNA) to identify the biological interaction between the gut ecosystem and its metabolites that could impact the immunotherapy response in non-small cell lung cancer (NSCLC) patients undergoing second-line treatment with anti-PD1. Metabolomic data were merged with operational taxonomic units (OTUs) from 16S RNA-targeted metagenomics and classified by chemometric models. The traits considered for the analyses were: (i) condition: disease or control (CTRLs), and (ii) treatment: responder (R) or non-responder (NR). Network analysis indicated that indole and its derivatives, aldehydes and alcohols could play a signaling role in GM functionality. WGCNA generated, instead, strong correlations between short-chain fatty acids (SCFAs) and a healthy GM. Furthermore, commensal bacteria such as , Rikenellaceae, , Peptostreptococcaceae, Mogibacteriaceae and Clostridiaceae were found to be more abundant in CTRLs than in NSCLC patients. Our preliminary study demonstrates that the discovery of microbiota-linked biomarkers could provide an indication on the road towards personalized management of NSCLC patients.
Topics: Akkermansia; Alcohols; Aldehydes; Antineoplastic Agents, Immunological; Bacteroides; Carcinoma, Non-Small-Cell Lung; Clostridiaceae; Databases, Genetic; Disease Progression; Drug Monitoring; Fatty Acids, Volatile; Gastrointestinal Microbiome; Gene Expression Regulation, Neoplastic; Gene Regulatory Networks; Humans; Immunotherapy; Indoles; Lung Neoplasms; Metabolome; Metagenomics; Peptostreptococcus; Precision Medicine; Programmed Cell Death 1 Receptor; RNA, Ribosomal, 16S; Signal Transduction
PubMed: 33227982
DOI: 10.3390/ijms21228730 -
Gut Sep 2020is associated with gastric inflammation, precancerous gastric atrophy (GA) and intestinal metaplasia (IM). We aimed to identify microbes that are associated with... (Randomized Controlled Trial)
Randomized Controlled Trial
OBJECTIVE
is associated with gastric inflammation, precancerous gastric atrophy (GA) and intestinal metaplasia (IM). We aimed to identify microbes that are associated with progressive inflammation, GA and IM 1 year after eradication.
DESIGN
A total of 587 -positive patients were randomised to receive eradication therapy (295 patients) or placebo (292 patients). Bacterial taxonomy was analysed on 404 gastric biopsy samples comprising 102 pairs before and after 1 year eradication and 100 pairs before and after 1 year placebo by 16S rRNA sequencing.
RESULTS
Analysis of microbial sequences confirmed the eradication of in treated group after 1 year. Principal component analysis revealed distinct microbial clusters reflected by increase in bacterial diversity (p<0.00001) after eradication. While microbial interactions remained largely unchanged after placebo treatment, microbial co-occurrence was less in treated group. , and were enriched while and were depleted in patients with persistent inflammation 1 year after eradication. A distinct cluster of oral bacteria comprising , , , and were associated with emergence and persistence of GA and IM. Probiotic was depleted in subjects who developed GA following eradication. Functional pathways including amino acid metabolism and inositol phosphate metabolism were enriched while folate biosynthesis and NOD-like receptor signalling decreased in atrophy/IM-associated gastric microbiota.
CONCLUSION
This study identified that gastric microbes contribute to the progression of gastric carcinogenesis after eradication.
Topics: Bacteria; Biopsy; Carcinogenesis; Disease Eradication; Disease Progression; Female; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metaplasia; Microbial Interactions; Middle Aged; Sequence Analysis, RNA; Stomach
PubMed: 31974133
DOI: 10.1136/gutjnl-2019-319826 -
Cureus Jun 2022Fish bone-induced pancreatitis is an uncommon cause of pancreatitis, with only a few reported cases in the literature. The patients with the highest risk for fish...
Fish bone-induced pancreatitis is an uncommon cause of pancreatitis, with only a few reported cases in the literature. The patients with the highest risk for fish bone-induced pancreatitis include those from cultures where unfilleted fish is a culinary delicacy. The etiology of foreign body-induced pancreatitis is very common, secondary to inflammation of the duodenal papilla or bile duct obstruction. CT imaging is key for visualization of the fish bone, as radiography rarely detects fish bones. Complications of fish bone-induced pancreatitis include thrombosis of the superior mesenteric vein, bacteremia (with ), pancreatic granuloma, and gastrointestinal perforation. Management of fish bone-induced pancreatitis includes either endoscopic resection or exploratory laparotomy, followed by supportive care until pancreatitis resolves. Here, we present a case of pancreatitis secondary to accidental fish bone ingestion, identified during upper gastrointestinal endoscopy and managed by bone removal and supportive care.
PubMed: 35891822
DOI: 10.7759/cureus.26191 -
Microbiology Spectrum Aug 2023The pivotal roles of gut microbiota in severe acute pancreatitis-associated acute lung injury (SAP-ALI) are increasingly revealed, and recent discoveries in the gut-lung...
Mechanisms of Qingyi Decoction in Severe Acute Pancreatitis-Associated Acute Lung Injury via Gut Microbiota: Targeting the Short-Chain Fatty Acids-Mediated AMPK/NF-κB/NLRP3 Pathway.
The pivotal roles of gut microbiota in severe acute pancreatitis-associated acute lung injury (SAP-ALI) are increasingly revealed, and recent discoveries in the gut-lung axis have provided potential approaches for treating SAP-ALI. Qingyi decoction (QYD), a traditional Chinese medicine (TCM), is commonly used in clinical to treat SAP-ALI. However, the underlying mechanisms remain to be fully elucidated. Herein, by using a caerulein plus lipopolysaccharide (LPS)-induced SAP-ALI mice model and antibiotics (Abx) cocktail-induced pseudogermfree mice model, we tried to uncover the roles of the gut microbiota by administration of QYD and explored its possible mechanisms. Immunohistochemical results showed that the severity of SAP-ALI and intestinal barrier functions could be affected by the relative depletion of intestinal bacteria. The composition of gut microbiota was partially recovered after QYD treatment with decreased / ratio and increased relative abundance in short-chain fatty acids (SCFAs)-producing bacteria. Correspondingly increased levels of SCFAs (especially propionate and butyrate) in feces, gut, serum, and lungs were observed, generally consistent with changes in microbes. Western-blot analysis and RT-qPCR results indicated that the AMPK/NF-κB/NLRP3 signaling pathway was activated after oral administration of QYD, which was found to be possibly related to the regulatory effects on SCFAs in the intestine and lungs. In conclusion, our study provides new insights into treating SAP-ALI through modulating the gut microbiota and has prospective practical value for clinical use in the future. Gut microbiota affects the severity of SAP-ALI and intestinal barrier function. During SAP, a significant increase in the relative abundance of gut pathogens (Escherichia, , Enterobacter, , ) was observed. At the same time, QYD treatment decreased pathogenic bacteria and increased the relative abundance of SCFAs-producing bacteria (, , , , ). In addition, The AMPK/NF-κB/NLRP3 pathway mediated by SCFAs along the gut-lung axis may play an essential role in preventing the pathogenesis of SAP-ALI, which allows for reduced systemic inflammation and restoration of the intestinal barrier.
Topics: Mice; Animals; Pancreatitis; NF-kappa B; NLR Family, Pyrin Domain-Containing 3 Protein; AMP-Activated Protein Kinases; Gastrointestinal Microbiome; Acute Disease; Prospective Studies; Acute Lung Injury; Fatty Acids, Volatile
PubMed: 37338348
DOI: 10.1128/spectrum.03664-22 -
Microorganisms Jun 2020Gallstone disease (GSD) has, for many years, remained a high-cost, socially significant public health problem. Over the past decade, a number of studies have been... (Review)
Review
Gallstone disease (GSD) has, for many years, remained a high-cost, socially significant public health problem. Over the past decade, a number of studies have been carried out-both in humans and in animal models-confirming the role of the microbiota in various sections of the gastrointestinal tract as a new link in the etiopathogenesis of GSD. The microbiome of bile correlates with the bacterial composition of saliva, and the microbiome of the biliary tract has a high similarity with the microbiota of the duodenum. Pathogenic microflora of the oral cavity, through mechanisms of immunomodulation, can affect the motility of the gallbladder and the expression of mucin genes ( ), and represent one of the promoters of stone formation in the gallbladder. The presence of infection contributes to the formation of gallstones and affects the occurrence of complications of GSD, including acute and chronic cholecystitis, cholangitis, pancreatitis. Intestinal bacteria (, and ) participating in the oxidation and epimerization of bile acids can disrupt enterohepatic circulation and lead to the formation of gallstones. At the same time, cholecystectomy due to GSD leads to the further transformation of the composition of the microbiota in various parts of the gastrointestinal tract, increasing the risk of developing stomach cancer and colorectal cancer. Further research is required to determine the possibility of using the evaluation of the composition of the microbiota of the gastrointestinal and biliary tracts as an early diagnostic marker of various gastroenterological diseases.
PubMed: 32498344
DOI: 10.3390/microorganisms8060835 -
Journal of Gastrointestinal Oncology Dec 2019Colorectal cancer (CRC) is a common cancer globally. It is a complex disease influenced by genetic and environmental factors. Early studies on familial cases have... (Review)
Review
Colorectal cancer (CRC) is a common cancer globally. It is a complex disease influenced by genetic and environmental factors. Early studies on familial cases have identified major genes involved in CRC, such as proto-oncogenes and , and tumour-suppressor genes and . These genes have provided valuable insight into the molecular pathogenesis of CRC, and some have made ways to clinical utility to help diagnose cancer syndromes, prognosticate oncological outcomes and predict treatment responses. While these genetic factors are important, recent studies have suggested contribution of microorganisms to colorectal carcinogenesis. Observational studies, animal experiments and translational works have identified several microorganisms as potential carcinogenic bacteria, such as and . With the advent of sequencing technology and bioinformatics, more genomic and metagenomic factors are being uncovered as important players in CRC carcinogenesis. This article aims to review recent genomic and metagenomic discoveries relating to CRC.
PubMed: 31949936
DOI: 10.21037/jgo.2019.06.04